Metabotropic glutamate autoreceptors on nerve terminals of crayfish muscle depress or facilitate release

Schramm, Marion; Dudél, J.

doi:10.1016/s0304-3940(97)00661-7

Cited by 17 publications

(17 citation statements)

References 11 publications

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“…2 and in most other experiments, autoinhibition reduced the average release. However, there is the complication that L‐Glu in particular activates an additional facilitatory receptor that masks some of the inhibition and sometimes even overcomes the inhibitory effect of Glu on average release (Schramm & Dudel, 1997; Dudel & Schramm, 2003; Dudel, 2004). Overall facilitation was seen in five of the 20 experiments summarized in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Actually, the experiments in Cl – ‐free solutions showed not only a block of autoinhibition and of the early surplus of releases but also a facilitation of release and a suppression of early releases. What remains after the block of autoinhibition is due to activation of the facilitating presynaptic Glu receptor (Schramm & Dudel, 1997). Apparently the activation of this receptor not only facilitates total release but also suppresses early releases.…”

Section: Discussionmentioning

confidence: 99%

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Glutamatergic autoinhibition of quantal release augments the early phase of releases after a depolarization pulse

Dudél

2006

Eur J of Neuroscience

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At the crayfish neuromuscular junction, glutamatergic autoinhibition of quantal excitatory postsynaptic current (qEPSC) release is mediated by a presynaptic DL-glutamate transporter and its associated Cl- conductance. I investigated whether it also affects the time course of release. qEPSCs were recorded with a perfused macroelectrode through which depolarization pulses and D- or L-glutamate could be applied to a terminal. In order to represent the time course of release, cumulative delays of qEPSCs were determined and scaled to a common final value. At 10 degrees C, on the application of D- or L-glutamate, release increased relative to the controls especially during its first millisecond, taking the mean of 20 experiments (P < 0.01). Also, in many single experiments the respective shifts in the time courses of release were highly significant. The relative surplus of early releases decreased with time constants tau1 of 86 micros and tau2 of 0.75 ms. At 0 degrees C, in the presence of glutamate, the surplus of early delays was increased relative to the controls to a significantly greater extent and for a longer time than at 10 degrees C. The tau1 of 240 micros was almost three times larger than at 10 degrees C. Autoinhibition was inactivated in Cl(-)-free solution. In such solutions the surplus of early releases also disappeared and the shortening of early delays reverted to a lengthening. Interaction of the inhibitory autoreceptor and its associated Cl- flow with the release machinery is discussed.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Glutamatergic autoinhibition of quantal release augments the early phase of releases after a depolarization pulse

Dudél

2006

Eur J of Neuroscience

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“…These findings suggested a role for NMDA-like receptors in the storage of long-term memory in the crab. In addition, the occurrence of these receptors in crustaceans has been often reported (Pfeiffer-Lynn and Glantz 1991;Parnas et al 1996;Burgess and Derby 1997;Schramm and Dudel 1997;Feinstein et al 1998). Here, the first experiments in this series were aimed at testing the effect of MK-801 on acquisition and consolidation of the extinction memory.…”

Section: Activity Of Nmda-like Receptors Is Required For Acquisitionmentioning

confidence: 99%

Memory is not extinguished along with CS presentation but within a few seconds after CS-offset

Pérez-Cuesta¹,

Hepp²,

Pedreira³

et al. 2007

Learn. Mem.

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Prior work with the crab's contextual memory model showed that CS-US conditioned animals undergoing an unreinforced CS presentation would either reconsolidate or extinguish the CS-US memory, depending on the length of the reexposure to the CS. Either memory process is only triggered once the CS is terminated. Based on these results, the following questions are raised. First, when is extinction memory acquired, if not along extinction training, and how long does it take? Second, can acquisition and consolidation of extinction memory be pharmacologically dissected? Here we address these questions performing three series of experiments: a first one aimed to study systematically the relationship between extinction and increasing periods of unreinforced CS presentations, a second one to determine the time boundaries of the extinction memory acquisition, and the third one to assay the requirement for protein synthesis and NMDA-like receptors of acquisition and consolidation of extinction memory. Our results confirm that it is CS-offset and not the mere retrieval (CS-onset) that triggers acquisition of extinction memory and that it is completed in less than 45 sec after CS-offset. In addition, protein synthesis is required for consolidation but not for acquisition of this memory and, conversely, NMDA-like receptor activity is required for its acquisition but not for its consolidation. Finally, we offer an interpretative scheme of our results and we discuss to what extent it could apply to multitrial extinction.

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“…Similar situations may occur in the variation and density of presynaptic glutamatergic autoreceptor subtypes that control the net response to glutamate in crayfish motor nerve terminals. In fact, Schramm and Dudel [42] reported that activation of glutamatergic autoreceptors of the crayfish NMJ could result in either depression or excitation of transmission, and they proposed that the varying proportions of glutamatergic receptor subtypes could account for their observations. It is established that vesicles can recycle empty at the Drosophila NMJ [43], so such a possibility might also occur at the crayfish NMJ.…”

Section: Table (1) Rrp and Docked Vesicle Analysismentioning

confidence: 99%

Presynaptic Depression in Phasic Motor Nerve Terminals and Influence of 5-HT on Vesicle Dynamics

Johnstone¹,

Kellie²,

Cooper³

2008

TONEURJ

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Synaptic depression that is induced by electrical stimulation of the glutamatergic neuromuscular junction (NMJ) of the crayfish can be offset by recruitment of vesicles from a presynaptic reserve pool. This recruitment occurs following treatment of the NMJ with serotonin (5-HT), which results in a delay in the onset of synaptic depression induced by high frequency stimulation. The results of this study demonstrate that the releasable vesicles are insufficiently replenished during high frequency stimulation and that the readily releasable pool of vesicles (RRP) can be enhanced by the reserve pool (RP) in the presence of 5-HT. Anatomical visualization of vesicular pools by transmission electron microscopy after depression or during 5-HT treatment showed no differences in the number of docked and RRP vesicles. We propose that the RRP vesicles can recycle empty and that a role for 5-HT might be to induce a rapid enhancement of synaptic transmission during synaptic fatigue.

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Metabotropic glutamate autoreceptors on nerve terminals of crayfish muscle depress or facilitate release

Cited by 17 publications

References 11 publications

Glutamatergic autoinhibition of quantal release augments the early phase of releases after a depolarization pulse

Glutamatergic autoinhibition of quantal release augments the early phase of releases after a depolarization pulse

Memory is not extinguished along with CS presentation but within a few seconds after CS-offset

Presynaptic Depression in Phasic Motor Nerve Terminals and Influence of 5-HT on Vesicle Dynamics

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